Melanin biosynthesis and its biological function as heat persistence in plantpathogens and other fungi

黑色素生物合成抑制剂，如扑草胺和敌草胺，影响稻瘟病菌分生孢子的形成。此外，在含有杀菌剂的培养基上的分生孢子增加了对热处理的敏感性。在杀菌剂抗性菌株中没有观察到杀菌剂诱导的耐热性降低，这表明黑化与耐热性之间存在相关性。粗枝脉孢菌的子囊、子囊孢子等性器官产生黑色色素，子囊孢子对热处理表现出较高的抗性。而黑色素缺失突变株per-1的子囊孢子对热处理敏感。经三环唑处理的野生型菌株积累了dhn-黑素的分流产物2-HJ。克隆了dhn-黑色素合成基因PKS、SDH和HNR，并进行了鉴定。转化野生型PKS基因的PER-1突变株恢复了黑色素生物合成能力和耐热性。Per-1突变株的PKS基因突变为^&lt；210&gt；Arg to Stop密码子。黑色素生物合成基因的转录是由受精诱导的，而不是由营养饥饿诱导的。

Melanin biosynthesis inhibitors, such as carpropamid and diclocymet, affected conidial formation in Pyricularia oryzae. In addition, the conidia on the medium containing fungicides increased the sensitivity to heat treatment. Reduced heat persistence induced by fungicides was not observed in fungicide resistant isolates, suggesting correlation between melanization and heat persistence. In Neurospora crassa, black pigment develops in sexual organs such as perithecia and ascospore, and ascospore showed high resistance to heat treatment. On the other hand, ascospore of the per-1 mutant, melanin deficient strain, was sensitive to heat treatment. The wild-type strain treated by tricyclazole accumulated 2-HJ, a shunt product of DHN-melanm. The DHN-melanin synthesis genes, such as PKS, SDH, and HNR, were clones and characterized. The per-1 mutant strain transformed with the wild-type PKSgene recovered the ability of melanin biosynthesis and heat resistance. The mutation within the PKSgene of the per-1 mutant strain was identified as ^<210>arg to stop codon. The transcription of melanin biosynthesis genes was induced by fertilization not by nutrient starvation in sexual cycle of N.crassa.